Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell RNAseq analysis of Igbpl1 treatment on microbead-induced glaucoma in mice

ABSTRACT: Single cell RNAseq analysis of Igbpl1 treatment on microbead-induced glaucoma in mice

PROVIDER: PRJNA940371 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23692441_1.fastq.gz	Fastqsanger.gz
	SRR23692441_2.fastq.gz	Fastqsanger.gz
	SRR23692442_1.fastq.gz	Fastqsanger.gz
	SRR23692442_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Single cell RNAseq analysis of Igbpl1 treatment on microbead-induced glaucoma in mice

2023-07-26 | GSE226456 | GEO

Functional Genomic Analysis of Glaucoma Pathogenesis Due to gmds Mutation in Zebrafish

Project description:Glaucoma, a major cause of irreversible blindness, is characterized by optic nerve damage and loss of retinal ganglion cells (RGC). SNPs in the GDP-MANNOSE 4,6-DEHYDRATASE (GMDS) gene have been linked to primary open-angle glaucoma (POAG) and treatment responses. The GMDS gene plays a critical role in fucosylation, a process essential for modifying glycoproteins and glycolipids, yet no mechanism for its role in glaucoma pathology has been described. Our study investigates the effects of gmds haploinsufficiency using a CRISPR/Cas9 induced mutation in zebrafish. RNA sequencing (RNAseq) analysis shows significant downregulation of stress response genes including those of the crystallin family, and increased expression of cell death genes in gmds heterozygous mutant eyes. These gene expression changes correlate with phenotypic alterations, including RGC layer thinning, RGC loss, and reduced optic nerve head width in adult gmds heterozygotes relative to wild type siblings. Our findings provide new insights into the role of GMDS in regulating eye function and suggests that GMDS may influence glaucoma risk by regulating the response to stress. This study provides a layer of functional evidence supporting the predictions made by previous GWAS findings, enhancing our understanding of the genetic basis of glaucoma. It highlights the potential of GMDS as a therapeutic target for mitigating glaucoma-related vision loss, opening new avenues for glaucoma research and treatment development.

2025-06-24 | GSE281042 | GEO

Single cell RNAseq analysis of wildtype and Igfbpl1-/- retina microglia

Project description:IGFBPL1 deficiency leads to progressive retinal neuron loss and phosphorylated Tau accumulation in the brain. To investigate the role of IGFBL1 in retina microglia homestasis and function. Total immune cells were sorted from wildtype and Igfbpl1-/- mice applied for single cell RNAseq analysis by 10X genomics technology. To further investigate the role of IGFBL1 in retina microglia homestasis and function. Total immune cells were sorted from microbead (MB)-induced glaucoma mice and glucoma mice treated with recombinant Igfbpl1 protein for single cell RNAseq analysis by 10X genomics technology. The scRNAseq data about MB-induced glaucoma refers to https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE226456 .

2021-06-05 | GSE176204 | GEO

Retinal sequencing results of glaucoma model in rats

Project description:Detecting differential genes between glaucoma model rats and normal group rats, studying gene pathways that may cause glaucoma visual impairment, and providing possible research directions for further prevention and treatment

2025-05-31 | GSE281891 | GEO

RNASeq of blood by Mesenchymal stem cells treatment on DNCB induced mice model

Project description:RNASeq of blood by Mesenchymal stem cells treatment on DNCB induced mice model

| PRJNA861127 | ENA

Uveitic glaucoma-like features in Yap conditional knockout mice

Project description:Glaucoma is a multifactorial neurodegenerative disease characterized by the progressive and irreversible degeneration of the optic nerve and retinal ganglion cells. Despite medical advances aiming at slowing degeneration down, around 40% of treated glaucomatous patients will undergo vision loss. It is thus of utmost importance to have a better understanding of the disease and to investigate more deeply its early causes. The transcriptional coactivator YAP, an important regulator of eye homeostasis, has recently drawn attention in the glaucoma research field. Here we show that Yap conditional knockout mice (Yap cKO), in which the deletion of Yap is induced in both Müller glia (i.e. the only retinal YAP-expressing cells) and the non-pigmented epithelial cells of the ciliary body, exhibit a breakdown of the aqueous-blood barrier, accompanied by a progressive collapse of the ciliary body. A similar phenotype is observed in human samples that we obtained from patients presenting with uveitis. In addition, aged Yap cKO mice harbor glaucoma-like features, including deregulation of key homeostatic Müller-derived proteins, retinal vascular defects, optic nerve degeneration and retinal ganglion cell death. Finally, transcriptomic analysis of Yap cKO retinas pointed to early-deregulated genes involved in extracellular matrix organization potentially underlying the onset and/or progression of the observed phenotype. Together, our findings reveal the essential role of YAP in preserving the integrity of the ciliary body and retinal ganglion cells, thereby preventing the onset of uveitic glaucoma-like features.

2024-01-01 | GSE251685 | GEO

RNASeq of skin tissues by Mesenchymal stem cells treatment on DNCB induced mice model

Project description:RNASeq of skin tissues by Mesenchymal stem cells treatment on DNCB induced mice model

| PRJNA862133 | ENA

Differentially expressed microRNAs in the aqueous humor of patients with exfoliation glaucoma or primary open-angle glaucoma

Project description:To better understand the molecular changes in the aqueous humor (AH) content with glaucoma, we analyzed the microRNA (miRNA) profiles of AH samples from patients with Primary Open Angle Glaucoma (POAG) and Exfoliation Glaucoma (XFG) compared to non-glaucoma controls.

2018-02-08 | GSE105269 | GEO

Gene Expression profiling in DBA/2J glaucoma

Project description:Glaucoma is a common ocular disorder that is a leading cause of blindness worldwide. It is characterized by the dysfunction and loss of retinal ganglion cells (RGCs). Although many studies have implicated various molecules in glaucoma, no mechanism has been shown to be responsible for the earliest detectable damage to RGCs and their axons in the optic nerve. Here, we show that the leukocyte transendothelial migration pathway is activated in the optic nerve head at the earliest stages of disease in an inherited mouse model of glaucoma. This resulted in proinflammatory monocytes entering the optic nerve prior to detectable neuronal damage. A 1-time x-ray treatment prevented monocyte entry and subsequent glaucomatous damage. A single x-ray treatment of an individual eye in young mice provided that eye with long-term protection from glaucoma but had no effect on the contralateral eye. Localized radiation treatment prevented detectable neuronal damage and dysfunction in treated eyes, despite the continued presence of other glaucomatous stresses and signaling pathways. Injection of endothelin-2, a damaging mediator produced by the monocytes, into irradiated eyes, combined with the other glaucomatous stresses, restored neural damage with a topography characteristic of glaucoma. Together, these data support a model of glaucomatous damage involving monocyte entry into the optic nerve. Genome-wide assessment of gene expression changes was performed in DBA/2J-Gpnmb+, DBA/2J mice and irradiated DBA/2J mice at 8.5 and 10.5 months of age.

2012-03-28 | GSE36833 | GEO

Glaucoma Exome Sequencing

Project description:Glaucoma Exome Sequencing

| PRJNA177503 | ENA